Characterization of serum-independent polymorphonuclear leukocyte chemotactic factors produced byPropionibacterium acnes

Inflammation ◽  
1980 ◽  
Vol 4 (3) ◽  
pp. 261-269 ◽  
Author(s):  
Guy F. Webster ◽  
James J. Leyden
Keyword(s):  
Polymorphonuclear Leukocyte ◽  
Chemotactic Factors

Characterization of human lymphocyte derived chemotactic factors for mononuclear phagocytes—I. Production and detection

1983 ◽  
Vol 20 (3) ◽  
pp. 317-324 ◽  
Author(s):  
Christiane Ramb ◽  
Ursula Malorny ◽  
Ulrich Feige ◽  
Clemens Sorg
Keyword(s):  
Human Lymphocyte ◽  
Mononuclear Phagocytes ◽  
Chemotactic Factors

Purification and characterization of neutrophil chemotactic factors of Streptococcus sanguis

1983 ◽  
Vol 758 (2) ◽  
pp. 181-186 ◽  
Author(s):  
Yoichiro Miyake ◽  
Tadashi Yasuhara ◽  
Kazuhiro Fukui ◽  
Hidekazu Suginaka ◽  
Terumi Nakajima ◽  
...  
Keyword(s):  
Purification And Characterization ◽  
Streptococcus Sanguis ◽  
Chemotactic Factors

scholarly journals Further Characterization of the epa Gene Cluster and Epa Polysaccharides of Enterococcus faecalis

2009 ◽  
Vol 77 (9) ◽  
pp. 3759-3767 ◽  
Author(s):  
Fang Teng ◽  
Kavindra V. Singh ◽  
Agathe Bourgogne ◽  
Jing Zeng ◽  
Barbara E. Murray
Keyword(s):  
Gene Cluster ◽  
Enterococcus Faecalis ◽  
Polymorphonuclear Leukocyte ◽  
Biofilm Formation ◽  
Oval Cells ◽  
Polysaccharide Biosynthesis ◽  
Polysaccharide Content ◽  
Shape Determination ◽  
Peritonitis Model

ABSTRACT We previously identified a gene cluster, epa (for enterocococcal polysaccharide antigen), involved in polysaccharide biosynthesis of Enterococcus faecalis and showed that disruption of epaB and epaE resulted in attenuation in translocation, biofilm formation, resistance to polymorphonuclear leukocyte (PMN) killing, and virulence in a mouse peritonitis model. Using five additional mutant disruptions in the 26-kb region between orfde2 and OG1RF_0163, we defined the epa locus as the area from epaA to epaR. Disruption of epaA, epaM, and epaN, like prior disruption of epaB and epaE, resulted in alteration in Epa polysaccharide content, more round cells versus oval cells with OG1RF, decreased biofilm formation, attenuation in a mouse peritonitis model, and resistance to lysis by the phage NPV-1 (known to lyse OG1RF), while mutants disrupted in orfde2 and OG1RF_163 (the epa locus flanking genes) behaved like OG1RF in those assays. Analysis of the purified Epa polysaccharide from OG1RF revealed the presence of rhamnose, glucose, galactose, GalNAc, and GlcNAc in this polysaccharide, while carbohydrate preparation from the epaB mutant did not contain rhamnose, suggesting that one or more of the glycosyl transferases encoded by the epaBCD operon are necessary to transfer rhamnose to the polysaccharide. In conclusion, the epa genes, uniformly present in E. faecalis strains and involved in biosynthesis of polysaccharide in OG1RF, are also important for OG1RF shape determination, biofilm formation, and NPV-1 replication/lysis, as well as for E. faecalis virulence in a mouse peritonitis model.

scholarly journals THE RELATIONSHIP OF THE CHEMOTACTIC BEHAVIOR OF THE COMPLEMENT-DERIVED FACTORS, C3a, C5a, AND C567, AND A BACTERIAL CHEMOTACTIC FACTOR TO THEIR ABILITY TO ACTIVATE THE PROESTERASE 1 OF RABBIT POLYMORPHONUCLEAR LEUKOCYTES

1972 ◽  
Vol 135 (2) ◽  
pp. 376-387 ◽  
Author(s):  
Elmer L. Becker
Keyword(s):  
Polymorphonuclear Leukocyte ◽  
Esterase Activity ◽  
Polymorphonuclear Leukocytes ◽  
Quantitative Difference ◽  
Chemotactic Activity ◽  
General Requirement ◽  
Chemotactic Factors ◽  
Relationship Of ◽  
The Relationship ◽  
Chemotactic Behavior

The inhibition profiles obtained when a series of p-nitrophenyl ethyl alkylphosphonates and of p-nitrophenyl ethyl chloroalkylphosphonates were used to interfere with the chemotactic activity of polymorphonuclear leukocytes stimulated by C3a, C5a, and bacterial factor were the same as found previously when C567 was the chemotactic agent. This indicates that as in the chemotactic activity induced by C567, an obligatory step in the chemotaxis caused by C3a, C5a, and bacterial factor is the activation of proesterase 1 of the rabbit polymorphonuclear leukocyte. C5a and C3a activate proesterase 1 of peripheral blood polymophonuclear leukocytes as measured by the increase of acetyl DL-phenylalanine ß-naphthyl esterase activity. Attempts to detect in a like manner the proesterase 1 of the same leukocytes using bacterial factor under varying circumstances have consistently failed. It is concluded that bacterial factor, for unknown reasons, is unable to activate proesterase 1 to the same extent as the complement-derived chemotactic factors. The hypothesis of there being a quantitative difference in the ability of bacterial factor to activate proesterase 1 compared with the complement-derived factors explains the previous observations that bacterial factor can not deactivate to itself or to the complement-derived factors, although these latter factors can deactivate to themselves, to each other, and to the bacterial factor. The quantitative difference in the ability of bacterial factor to activate proesterase 1 compared to the complement-derived factors is also associated with and explains the finding that the maximal chemotactic activity attainable when bacterial factor is the chemotactic agent is distinctly less than that obtained using either C3a, C5a, or C567. These results indicate that the activation of proesterase 1 is a general requirement for the chemotactic activity of rabbit polymorphonuclear leukocytes with known macromolecular chemotactic agents and suggest that under several different circumstances the level of chemotactic activity attained is related to the degree of such activation.

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